This project will provide a foundation for future investigations regarding the optimization of peak bone mass obtained during adolescence. Osteoporosis, once thought to be a natural part of aging among women, is no longer considered age- or gender-dependent. Low bone mass in young women has emerged as a crucial factor that may contribute to the development of osteoporosis. Studies have reported bone densities in young athletic women similar to 51-year-old women. In a recent study, 72% of amenorrheic athletes had bone densities that met the diagnostic criterion for osteopenia or osteoporosis. Multiple factors have been found to correlate with low bone mass in young women including low estrogen scores and increased age at menarche. Therefore, the effect of delayed estrogen levels during bone development may decrease the peak bone mass in young adults and lead to an increase risk of fractures later in life. Few studies have been focused on the relationship between delayed menarche and peak bone mass. The aim of this research is to develop an animal model that will delay menarche and, in turn, alter peak bone mass. Rats will be injected with GnRH antagonists to delay the increase of estrogen levels prior to reproductive maturation. GnRH antagonists will be withdrawn at age 8 weeks. Bone slices of rat tibiae and lumbar spine will be analyzed using histomorphometric measurements and compared between groups. Cross-sectional slices of the tibia midshaft will be analyzed. Specifically, cross-sectional area and the polar moment of inertia will be measured. Ash content values of bones will be measured to assess bone quality (mineral content). Blood will be taken from the tail vein bi-weekly and serum estrogen levels (pg/mL) will be measured using an estradiol ultra-sensitive double antibody RIA. LH and FSH measures will be measured using ELISA kits. All groups will be sacrificed by anesthesia overdose at 24 weeks of age. A one-way ANOVA will be used for this study with a significance level of 0.05.